TABLE 1.

Experimental models used, the protocols, and the role exercised by HIF in studies involved in the article.

Model of the study	Methods	Outcome and experimental evidence	References
Mouse model with high-fat diet induced atherosclerosis	The lesion formation of EC-Hif1a-/- mice and wild type were determined after partial carotid ligation and HFD feeding.	EC-Hif1a-/- mice generated reduced lesion area compared to EC-Hif1a + / + mice.	Akhtar et al., 2015
Mouse aortae endothelial cell model after HFD feeding	Monocyte adhesion to MAECs was determined after the stimulation of LPA20:4, LPA18:0, moxLDL or nLDL.	The moxLDL-and LPA20:4-induced monocyte adhesion was abolished by silencing Hif-1a in MAECs. Upregulation of HIF1a helps MoxLDL-derived unsaturated LPAs promote CXCL1-dependent monocytes adhesion.	Akhtar et al., 2015
Mouse aortae endothelial cell model after HFD feeding	Endothelial cell proliferation was measured between Hif-1a silencing group and the control group.	The proliferation of ECs was decreased in gene silencing group, demonstrating that EC proliferation is regulated by Hif-1a.	Feng et al., 2017
Mouse pulmonary hypertension model induced by hypoxia-induced mitogenic factor (HIMF) injection	The level of medial thickening was determined between HIF-1α+/+ and HIF-1α± group after HIMF injection.	An obvious medial thickening was induced by HIMF in the HIF-1α+/+ group, while the process was dismissedin the HIF-1α± group, indicating the regulation effect of HIF-1α in the PH development.	Johns et al., 2016
Mouse model by normoxia or chronic hypoxia (10% O2) for 30 days	HIF-1α deletion was performed in 2 ways on model group mice, followed by normoxia and chronic hypoxia exposure to all groups.	HIF-1α-SMM-Cre mice generated decreased arterial wall thickness, while the control group mice developed significant vascular remodeling in arteries, showing HIF-1α as an important part in vascular remodeling regulation.	Ball et al., 2014